Atrial fibrillation has been characterized by a rapid irregular heartbeat and can be intermittent or permanent in nature. Atrial fibrillation (AF) is caused by a dysfunction of the heart tissue or nodes, by a dysfunction of the autonomic nervous system or by a combination thereof. Individual heart cells are capable of beating outside of the control of the autonomic system. Sometimes, agglomerations of very active cells form and create a focus which results in ectopic beats, namely beats that originate at a location within the heart other than the sino-atrial (SA) node. The junction between the left atrium and the pulmonary vein may be a common location where ectopic beats originate from cell agglomerations.
If left untreated, ectopic beats may become very frequent and run together with one another, thereby creating atrial fibrillation. Atrial fibrillation involves a chaotic movement of electrical impulses across the atria. Atrial fibrillation may lead to a loss of synchrony between the atria and the ventricles. Once an episode of atrial fibrillation has begun, the atria may quiver or fibrillate at a rate as high as 300-600 times per minute. Such high fibrillation causes a very inefficient filling and emptying process of the atria. The chaotic quivering behavior of the atria may then be transferred to the ventricles and cause the ventricles to lose a regular rhythmic behavior and begin to contract fast and/or in a totally irregular manner. This type of chaotic transfer to the ventricles often gives rise to the fast and irregular pulse rate felt during an AF episode (e.g. between 90 and 160 per minute).
Atrial flutter is another atrial arrhythmia that is characterized by rapid atrial behavior. Atrial flutter may sometimes go unnoticed, yet its onset is often marked by characteristic sensations of regular palpitations. These sensations may last until the episode resolves or until the heart rate becomes under control. Atrial flutter is usually well tolerated initially, as the high heart rate is similar to the heart rate that a person experiences during normal exercise. However, some patients with underlying heart disease or poor exercise tolerance may rapidly develop adverse symptoms which can include shortness of breath, chest pains, light headedness or dizziness, nausea and, in some patients, nervousness and feelings of impending doom. Prolonged fast flutter may lead to decompensation with loss of normal function and potential heart failure. Prolonged fast flutter may manifest as breathlessness, nocturnal breathlessness, swelling of the lungs and swelling of the abdomen.
IMDs detect various arrhythmias such as atrial fibrillation (AF), atrial flutter (A-Flutter), and atrial tachycardia (AT) (hereafter collectively atrial arrhythmias). Arrhythmias are detected based on one or more of ventricular rate, rate stability, and the morphology of the cardiac signal. However, conventional algorithms for detecting arrhythmias experience certain limitations. For example, conventional AF detection algorithms that are based on rate stability may become confounded when an atrial tachyarrhythmia drives a ventricle at a high, but very stable rate. When a patient experiences atrial tachyarrhythmia having a stable rate, the AF detection algorithm may classify the events merely as high rate normal sinus events. Thus, the AF detection algorithm may not declare the events to be pathologic (non-physiologic) and may not deliver a therapy. Further, conventional algorithms may not correctly classify atrial fibrillation that exhibits rate dependent changes in the QRS complex. When a patient experiences atrial tachyarrhythmia having rate dependent changes in the QRS complex, the morphology detection algorithm may classify the events merely as physiologic events and thus, may not declare the events to be pathologic.
At least certain limitations of conventional detection algorithms extend, in part, from the fact that the algorithms analyze IEGM signals from various combinations of electrodes within and surrounding the heart. IEGM signals are a direct indicator of the electrical activity within the tissue of the heart. While heart tissue electrical activity is a good surrogate of heart electrical behavior, the electrical activity is not directly correlated to the resultant actual “mechanical” output of the heart. The mechanical output of the heart constitutes the actual cardiac output (CO) of the heart. Cardiac output represents a volume of blood that is ejected from the heart over a period of time. For example, the cardiac output may be quantified in terms of the stroke volume (SV) (ml/heart beat) times the heart rate (beats/minute). While IEGM signals are a good approximation of cardiac output, IEGM signals are not a direct surrogate of hemodynamic performance.
Heretofore, various intra-cardiac indicators (ICI) have been proposed for monitoring cardiac activity, such as heart sounds, blood pressure, and the like. It has also been proposed to monitor certain types of intra-cardiac impedance (within the heart) to derive hemodynamic performance. Intra-cardiac impedance represents impedance that is measured between electrodes that are located within the heart (intra-cardiac electrodes). For example, the intra-cardiac electrodes may be located within the right atrium and the right ventricle with the intra-cardiac impedance measured therebetween. The intra-cardiac electrodes define an intra-cardiac impedance vector that extends through one or both of the atrium and ventricle. The entire intra-cardiac impedance vector or at least a substantial majority of the intra-cardiac impedance vector lies within, and extends through, the blood pool in the chambers of the heart.
Intra-cardiac impedance exhibits a high value when the associated heart chamber(s) are in a systole state. The intra-cardiac impedance exhibits a low value when the associated heart chamber(s) are in a diastole state. As the corresponding heart chambers transition between systole and diastole, the impedance waveform moves between peaks and valleys. The intra-cardiac impedance waveform has not proven to be a good surrogate of stroke volume or hemodynamic performance. One limitation of the intra-cardiac impedance waveform arose from the fact that the intra-cardiac impedance vector extends through multiple chambers of the heart. Thus, each measurement of intra-cardiac impedance includes components from individual chambers of the heart, not the overall cooperative effect of all of the heart chambers.
Presently, implantable devices have been proposed that record IEGM signals when AF episodes are identified. However, the IEGM signals alone do not entirely reflect the true mechanical hemodynamic performance of the heart. For example, the IEGM signals may indicate that a substantial AF episode occurred, yet the episode may be of a nature in which the hemodynamic performance has not been significantly diminished from normal hemodynamic performance. Alternatively, in certain AF episodes, the corresponding IEGM signal may indicate the episode to be of nominal significance, while the underlying mechanical behavior of the heart results in substantial diminished hemodynamic performance. IMDs that record only IEGM signals do not necessarily inform a physician of the true mechanical behavior of the heart during a corresponding episode. Given the potential limited correlation between IEGM signals and mechanical hemodynamic performance, it has been difficult to assess an appropriate therapy or ablation.
A need exists for an IMD that stores information directly correlated to the hemodynamic performance of the heart during AF and atrial flutter events.
A need remains for improved techniques for implantable medical devices to detect and accurately characterize atrial fibrillation and atrial flutter.